In the Finale we examine to what extent Causal Mechanism can be seen as a descendant of the original notion of mechanism developed in seventeenth century, by examining possible extensions of the seventeenth-century notion of mechanism and discussing whether they can be used to characterise mechanism as a concept-in-use. We identify two conditions that a biological explanation has to satisfy in order to count as mechanistic, both of which were central in Old Mechanism: the condition of intelligibility and the condition of the priority of the parts over the whole. We use these two conditions to distinguish between two notions of mechanism: a more narrow one that incorporates both the intelligibility condition and the condition of the priority of the parts and a broader one that incorporates only the intelligibility condition and is thus a weakened form of mechanism. We claim that an account of mechanism as a concept-in-use requires the weakened notion, which when viewed in terms of Causal Mechanism has nevertheless enough content so that it can be seen as a descendant of the original concept.

Chapter 1 examines the relationship between Old and New Mechanism and uses it to illuminate the relations between metaphysical and methodological conceptions of mechanism. This historical examination will directly motivate our new deflationary account of mechanism developed in the subsequent chapters. We start by focusing on the role of mechanistic explanation in seventeenth-century scientific practice, by discussing the views of René Descartes, Christiaan Huygens, Gottfried Wilhelm Leibniz and Robert Boyle, and the attempted mechanical explanations of gravity by Descartes and Ηuygens. We thereby illustrate how the metaphysics of Old Mechanism constrained scientific explanation. We then turn our attention to Isaac Newton’s critique of mechanism. The key point is that Newton introduced a new methodology that freed scientific explanation from the metaphysical constraints of the older mechanical philosophy. Last, we draw analogies between Newton’s critique of Old Mechanism and our critique of New Mechanism. The main point is that causal explanation in the sciences is legitimate even if we bracket the issue of the metaphysics of mechanisms.

In Chapter 9 we present and defend a causal account of multilevel mechanistic explanation by examining various case studies from biology. We argue that two key consequences of Causal Mechanism are (1) that levels and mechanisms are distinct notions and (2) that levels of multilevel explanations are levels of composition. This view is in stark contrast to Craver’s account, according to which levels in multilevel explanations are levels of mechanisms and multilevel explanations are instances of constitutive explanations. A key claim of the chapter is that whatever contributes to the phenomenon is part of the same pathway; but causal pathways can contain entities from multiple levels of composition. In order to motivate and illustrate our view, we use various examples from biology and medicine. We criticise some common views associated with the picture of a hierarchy of mechanistic levels and argue that our view allows for causation at higher levels.

This chapter offers a framework for understanding mechanistic explanations of psychiatric disorders in terms of altered activities in a heterarchical network of control mechanisms. This differs both from approaches that seek to characterize the mechanism responsible for producing the disease state and those that attribute the disease state to broken mechanisms. Control mechanisms operate on soft constraints in other mechanisms and thereby alter their operation. Although often viewed as hierarchical, the brain is organized as a heterarchical network, with many control mechanisms operating on the same controlled mechanisms and no chief executive. This poses challenges for attempts to understand the ramifications of altered functioning of components of the network. Using a recent example of research showing the effects of modifying the activity of proteins within the circadian clock on depression-like behavior in mice, this chapter illustrates how progress might be made as well as the challenges faced in explaining psychiatric disorders.